NAVLE Multisystemic

Equine Metabolic Syndrome Study Guide

Equine Metabolic Syndrome (EMS) is a collection of clinical abnormalities characterized by insulin dysregulation (ID) as the core feature, with regional or generalized adiposity and predisposition to hyperinsulinemia-associated laminitis (HAL).

Overview and Clinical Importance

Equine Metabolic Syndrome (EMS) is a collection of clinical abnormalities characterized by insulin dysregulation (ID) as the core feature, with regional or generalized adiposity and predisposition to hyperinsulinemia-associated laminitis (HAL). EMS represents over 90% of all laminitis cases in the general equine population, making it the leading cause of laminitis. Understanding EMS pathophysiology, diagnosis, and management is essential for NAVLE success and clinical practice.

The condition shares similarities with human metabolic syndrome (Type 2 diabetes risk factors) but differs in that the primary clinical consequence in horses is laminitis rather than cardiovascular disease. EMS was first formally described by Johnson in 2002 and has since become one of the most important endocrine disorders in equine practice.

High-YieldFor NAVLE, remember that insulin dysregulation is the CORE component of EMS. Obesity alone is NOT sufficient to diagnose EMS, and lean horses CAN have EMS. The diagnosis requires documentation of insulin dysregulation.
Component Description
Basal Hyperinsulinemia Elevated resting insulin concentrations greater than 20 microIU/mL (some laboratories use greater than 50 microIU/mL)
Postprandial Hyperinsulinemia Exaggerated and prolonged insulin response to oral carbohydrates; detected via OST or oral glucose test
Tissue Insulin Resistance Inadequate tissue response to insulin; may be hepatic, peripheral (skeletal muscle), or both

Pathophysiology

Insulin Dysregulation

Insulin dysregulation (ID) is the central feature of EMS and can manifest as one or more of the following: basal (resting) hyperinsulinemia, postprandial or post-challenge hyperinsulinemia, and tissue insulin resistance (hepatic and/or peripheral). Hyperinsulinemia is the most important pathophysiologic feature because it directly causes laminitis.

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